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The War is Over: We Won!

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Here is the abstract from a Nature Review: Genetics paper:

The recent increase in genomic data is revealing an unexpected perspective of gene loss as a pervasive source of genetic variation that can cause adaptive phenotypic diversity. This novel perspective of gene loss is raising new fundamental questions. How relevant has gene loss been in the divergence of phyla? How do genes change from being essential to dispensable and finally to being lost? Is gene loss mostly neutral, or can it be an effective way of adaptation? These questions are addressed, and insights are discussed from genomic studies of gene loss in populations and their relevance in evolutionary biology and biomedicine.

Many years ago, I predicted that modern genome sequencing would eventually prove one side of the argument to be right. This review article indicates that ID is the correct side of the argument. What they describe is essentially what ID scientist, Michael Behe, has termed the “First Principle of Adaptation.” (Which says that the organism will basicaly ‘break something’ or remove something in order to adapt) This paper ought to be the death-knell of Darwinism, and, of course, “neo-Darwinism,” but, even the authors who report this new “perspective” have not changed their Darwinian perspective. Somehow, they will find a way to tell us that the Darwinian ‘narrative’ always had room in it for this kind of discovery. As Max Planck said, and I paraphrase, “a theory does not prove itself right; it’s just that the scientists who opposed it eventually die.”

Here is basically the first page of the article (which is all I had access to):

Great attention has in the past been paid to the mechanisms of evolution by gene duplication (that is, neofunctionalization and subfunctionalization). By contrast, gene loss has often been associated with the loss of redundant gene duplicates without apparent functional consequences, and therefore this process has mostly been neglected as an evolutionary force. However, genomic data, which is accumulating as a result of recent technological and methodological advances, such as next-generation sequencing, is revealing a new perspective of gene loss as a pervasive source of genetic change that has great potential to cause adaptive phenotypic diversity.

Two main molecular mechanisms can lead to the loss of a gene from a given genome. First, the loss of a gene can be the consequence of an abrupt mutational event, such as an unequal crossing over during meiosis or the mobilization of a transposable or viral element that leads to the sudden physical removal of the gene from an organisms’ genome. Second, the loss of a gene can be the consequence of a slow process of accumulation of mutations during the pseudogenitzation that follows an initial loss-of-function mutation. This initial mutation can be caused by nonsense mutations that generate truncated proteins, insertions or deletions that cause a frameshift, missense mutations that affect crucial amino acid positions, changes involving splice sites that lead to aberrant transcripts or mutations in regulatory regions that abolish gene expression. In this Review, the term ‘gene loss’ is used in a broad sense, not only referring to the absence of a gene that is identified when different species are compared, but also to any allelic variant carrying a loss-of-function (that is, non-functionalization) mutation that is found within a population.

Here, we address some of the fundamental questions in evolutionary biology that have emerged from this novel perspective of evolution by gene loss. Examples from all life kingdoms are covered, from bacteria to fungi and from plants to animals, including key examples of gene loss in humans. We review how gene loss has affected the evolution of different phyla and address key questions, including how genes can become dispensable, how many of our current genes are actually dispensable, how patterns are biased, and whether the effects of gene loss are mostly neutral or whether gene loss can actually be an effective way of adaptation.

So, let’s translate what they’re saying here: “speciation” (their term is “phenotypic adaptation”) is the result of a LOSS of INFORMATION! This points, of course, to the “front-loading” of the LCA of the various branches of the so-called “Tree of Life.” Absolute bad news for Darwinism. We no longer say: “Another day; another bad day for Darwinism.” We now say: “Another day since the time Darwinism was disproved.”

This is what one of the authors has to say in an interview:

“The genome sequencing of very different organisms has shown that gene loss has been a usual phenomenon during evolution in all life cycles. In some cases, it has been proven that this loss might mean an adaptive response towards stressful situations when facing sudden environmental changes” says Professor Cristian Cañestro.

“In other cases, there are genetic losses –says Cañestro- which even though they are neutral per se, have contributed to the genetic and reproductive isolation among lineages, and thus, to speciation, or have rather participated in the sexual differentiation in contributing to the creation of a new Y chromosome. The fact that genetic loss patterns are not stochastic but rather biased in the lost genes[pav: IOW, this is where you’re going to find the genomic differences between species you compare] (depending on the kind of function of the gen or its situation in the genome in different organism groups) stresses the importance of the genetic loss in the evolution of the species.

There you have it: “evolution” through “gene loss.” I.e., “evolution” through “loss of information.” Evolution does not PRODUCE “information”; it DESTROYS “information”. You can read about in the book: “Genetic Entropy.”

In sum: the war is over, and we won! Congratulations everyone!

Comments
Has anybody read vjtorley's June 6th "Consider the opossum: the evidence for common descent" thread? Apparently all of us mammals have lost our genes for making egg yolks. Are we thus doomed?MatSpirit
June 22, 2016
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Alternative splicing is a very big part of what we're discussing here, and yet it doesn't seem to factor into the notion of "de novo" gene. Thanks for the citations.PaV
June 22, 2016
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Of related note to ORFan genes. Alternative splicing is very different between species. Even very different between chimps and humans:
Evolution by Splicing - Comparing gene transcripts from different species reveals surprising splicing diversity. - Ruth Williams - December 20, 2012 Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,, A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species. On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,, http://www.the-scientist.com/?articles.view%2FarticleNo%2F33782%2Ftitle%2FEvolution-by-Splicing%2F Gene Regulation Differences Between Humans, Chimpanzees Very Complex – Oct. 17, 2013 Excerpt: Although humans and chimpanzees share,, similar genomes, previous studies have shown that the species evolved major differences in mRNA (messenger RNA) expression levels.,,, http://www.sciencedaily.com/releases/2013/10/131017144632.htm ,,,Alternative splicing,,, may contribute to species differences - December 21, 2012 Excerpt: After analyzing vast amounts of genetic data, the researchers found that the same genes are expressed in the same tissue types, such as liver or heart, across mammalian species. However, alternative splicing patterns—which determine the segments of those genes included or excluded—vary from species to species.,,, The results from the alternative splicing pattern comparison were very different. Instead of clustering by tissue, the patterns clustered mostly by species. "Different tissues from the cow look more like the other cow tissues, in terms of splicing, than they do like the corresponding tissue in mouse or rat or rhesus," Burge says. Because splicing patterns are more specific to each species, it appears that splicing may contribute preferentially to differences between those species, Burge says,,, Excerpt of Abstract: To assess tissue-specific transcriptome variation across mammals, we sequenced complementary DNA from nine tissues from four mammals and one bird in biological triplicate, at unprecedented depth. We find that while tissue-specific gene expression programs are largely conserved, alternative splicing is well conserved in only a subset of tissues and is frequently lineage-specific. Thousands of previously unknown, lineage-specific, and conserved alternative exons were identified; http://phys.org/news/2012-12-evolution-alternative-splicing-rna-rewires.html
Moreover, alternative splicing allows for the same gene to code for multiple different protein products:
Time to Redefine the Concept of a Gene? - 2012 Excerpt: As detailed in my second post on alternative splicing, there is one human gene that codes for 576 different proteins, and there is one fruit fly gene that codes for 38,016 different proteins! While the fact that a single gene can code for so many proteins is truly astounding, we didn’t really know how prevalent alternative splicing is. Are there only a few genes that participate in it, or do most genes engage in it? The ENCODE data presented in reference 2 indicates that at least 75% of all genes participate in alternative splicing. They also indicate that the number of different proteins each gene makes varies significantly, with most genes producing somewhere between 2 and 25. http://networkedblogs.com/BYdo8 Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 - published online May 2013 Excerpt: In the last decade, we have discovered still another aspect of the multi- dimensional genome. We now know that DNA sequences are typically “ poly-functional” [38]. Trifanov previously had described at least 12 genetic codes that any given nucleotide can contribute to [39,40], and showed that a given base-pair can contribute to multiple overlapping codes simultaneously. The first evidence of overlapping protein-coding sequences in viruses caused quite a stir, but since then it has become recognized as typical. According to Kapronov et al., “it is not unusual that a single base-pair can be part of an intricate network of multiple isoforms of overlapping sense and antisense transcripts, the majority of which are unannotated” [41]. The ENCODE project [42] has confirmed that this phenomenon is ubiquitous in higher genomes, wherein a given DNA sequence routinely encodes multiple overlapping messages, meaning that a single nucleotide can contribute to two or more genetic codes. Most recently, Itzkovitz et al. analyzed protein coding regions of 700 species, and showed that virtually all forms of life have extensive overlapping information in their genomes [43]. 38. Sanford J (2008) Genetic Entropy and the Mystery of the Genome. FMS Publications, NY. Pages 131–142. 39. Trifonov EN (1989) Multiple codes of nucleotide sequences. Bull of Mathematical Biology 51:417–432. 40. Trifanov EN (1997) Genetic sequences as products of compression by inclusive superposition of many codes. Mol Biol 31:647–654. 41. Kapranov P, et al (2005) Examples of complex architecture of the human transcriptome revealed by RACE and high density tiling arrays. Genome Res 15:987–997. 42. Birney E, et al (2007) Encode Project Consortium: Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project. Nature 447:799–816. 43. Itzkovitz S, Hodis E, Sega E (2010) Overlapping codes within protein-coding sequences. Genome Res. 20:1582–1589. http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0006
Moreover, "Alternative splicing can produce variant proteins and expression patterns as different as the products of different genes."
Frequent Alternative Splicing of Human Genes – 1999 Excerpt: Alternative splicing can produce variant proteins and expression patterns as different as the products of different genes. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC310997/ Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing - 2016 In Brief Alternatively spliced isoforms of proteins exhibit strikingly different interaction profiles and thus, in the context of global interactome networks, appear to behave as if encoded by distinct genes rather than as minor variants of each other.,,, Page 806 excerpt: As many as 100,000 distinct isoform transcripts could be produced from the 20,000 human protein-coding genes (Pan et al., 2008), collectively leading to perhaps over a million distinct polypeptides obtained by post-translational modification of products of all possible transcript isoforms (Smith and Kelleher, 2013). http://iakouchevalab.ucsd.edu/publications/Yang_Cell_OMIM_2016.pdf
Thus, since alternative splicing is very different between different species, even very different between chimps and humans, and since alternative splicing produces up to a million polypeptides that appear "as if encoded by distinct genes rather than as minor variants of each other", then it is very reasonable to conclude that the "ORFan gene problem" is actually far more problematic than Darwinists pretend that it is. Supplemental notes:
Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 - May 2013 Conclusions: Our analysis confirms mathematically what would seem intuitively obvious - multiple overlapping codes within the genome must radically change our expectations regarding the rate of beneficial mutations. As the number of overlapping codes increases, the rate of potential beneficial mutation decreases exponentially, quickly approaching zero. Therefore the new evidence for ubiquitous overlapping codes in higher genomes strongly indicates that beneficial mutations should be extremely rare. This evidence combined with increasing evidence that biological systems are highly optimized, and evidence that only relatively high-impact beneficial mutations can be effectively amplified by natural selection, lead us to conclude that mutations which are both selectable and unambiguously beneficial must be vanishingly rare. This conclusion raises serious questions. How might such vanishingly rare beneficial mutations ever be sufficient for genome building? How might genetic degeneration ever be averted, given the continuous accumulation of low impact deleterious mutations? http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0006 Unexpected features of the dark proteome – Oct. 2015 We surveyed the “dark” proteome–that is, regions of proteins never observed by experimental structure determination and inaccessible to homology modeling. For 546,000 Swiss-Prot proteins, we found that 44–54% of the proteome in eukaryotes and viruses was dark, compared with only ~14% in archaea and bacteria. Surprisingly, most of the dark proteome could not be accounted for by conventional explanations, such as intrinsic disorder or transmembrane regions. Nearly half of the dark proteome comprised dark proteins, in which the entire sequence lacked similarity to any known structure. Dark proteins fulfill a wide variety of functions, but a subset showed distinct and largely unexpected features, such as association with secretion, specific tissues, the endoplasmic reticulum, disulfide bonding, and proteolytic cleavage. Dark proteins also had short sequence length, low evolutionary reuse, and few known interactions with other proteins. These results suggest new research directions in structural and computational biology. http://www.pnas.org/content/early/2015/11/16/1508380112
bornagain77
June 22, 2016
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Bob: Let me add that the way "de novo" is used in the literature amounts to equivocation. "De novo" means, more or less, something that is utterly new. When you have a piece from here, and a backwards piece from over there, that's not "de novo." It only helps to obfuscate things. Here, for example, is the very first sentence of an abstract from April of last year:
The origin of novel protein-coding genes de novo was once considered so improbable as to be impossible. In less than a decade, and especially in the last five years, this view has been overturned by extensive evidence from diverse eukaryotic lineages.
This sloppiness is unfortunately not uncommon in evolutionary literature.PaV
June 22, 2016
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Bob: I'm now wondering if there is equivocation going on within the literature itself. In the article I've cited, "novel" means that there is no connection to annotated sequences. To me this means that the gene is entirely new. It the paper you cited, the two terms seemed to be used in the opposite sense. So, to me, I'm using "novel" to mean that it is a gene that has no connection to already known, and annotated, sequences, and so cannot represent a product of duplication and degradation, or inversion.PaV
June 22, 2016
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PaV - you're clearly not using "de novo" and "novel" in the way they are used in the literature to describe genes, so can you explain what you mean by these terms please.Bob O'H
June 22, 2016
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Bob O'H:
PaV – wrt novel genes, once more google is your friend. Again, first page of results.
Couple of problems, Bob: first, what they consider to be "novel" genes, are really "de novo" genes. Second, which confirms the first point, here's what they say:
In Table 1 is summarized the information on a sample of novel genes that reveals a picture of the events involved in their origin and their function. The sample is limited to genes that originated less than 50 million years ago to avoid confounding events of origination with effects of later evolution;. . .
So, what has really "evolved" since 50 million years ago? Not much, and mostly mammals. And they study flies mostly. Sorry, this doesn't help your cause.
You’re still punting the problem of gene loss/gain, so I guess we’re done there. And I still haven’t seen any maths from you about overcoming long odds, so I guess we’re done there too.
Duplicating a gene is not a gene "gain." They have genomic sequence data that demonstrates--not just theorizes--that what differentiates species is the "loss" of genes. You'll just have to learn to live with it. As to the maths, it is you who must provide the recipe for overcoming long odds, not me. I still await. To simply grandstand and say "evolution" happened, and therefore long odds were overcome, is to simply put the cart before the horse. This is convincing to no one.PaV
June 22, 2016
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This statement from rvb8 sums up the whole debate nicely: "It seems that everyone here is hell bent on asking, ‘then why are we here, why are we so special?’ If this is your question, then it sadly fails to understand Darwinian Evolution. We reproduce sexually because we inherited this method from ancient ancestors. The ligitimate question of why we went down this evolutionarily less efficient method, is what science is trying to answer." In other words, Darwinian evolution has become truly an unquestionable religion. It has come to the point of being able to substitute the word "God" for evolution and it would not read any differently. Of course if we are good scientists we must question why something happens. Any scientific theory must hold up to all challenges. So if we cannot explain humans through RM&NS then those mechanisms are falsified for our existence and the whole theory fails. Yet we are told we reproduce sexually because we had ancestors who did. It's all an a priori assumption. Do not dare question the sacred evolutionary tale! Prove how our ancestors developed sexual reproduction and prove we actually could arise through chance from those ancestors. I was never asking why humans reproduce sexually, I was asking why any organism came about from an asexual ancestor through accident to reproduce sexually, it makes no sense by the definition of what evolution is about.Dr JDD
June 22, 2016
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rvb8 @88
You are correct HeKS, asexual reproduction is far more successful than sexual reproduction. That is why some plants, and some fungi, and all archaebacteria, eubacteria, and protists are far more abundent and therefore evolutionarily successful than us. It seems that everyone here is hell bent on asking, ‘then why are we here, why are we so special?’ If this is your question, then it sadly fails to understand Darwinian Evolution.
Did you actually see me say anything like that? No, you didn't. In fact, you have sadly failed to understand my point. My point is actually the opposite of what you've suggested. My point is that because Darwinian evolution is held to be a purposeless process lacking in any goals, evolutionary explanations for why some biological feature evolved are typically empty and misleading, because there is no reason that any biological feature evolved. There are only possible reasons why already evolved, functional features might be selected for. The thing is, in my experience, most casual believers in evolution ultimately think of evolution as a purposeful process. They think this because 1) they are constantly given teleological explanations for why biological features evolved (e.g. Feature A evolved because it has benefit X), and 2) their common sense tells them that 'just because' is an insufficient explanation for how a complex system could have arisen and been in a position to be selected for in the first place. These kinds of teleological explanations are common among science popularizers as well. For example, Bill Nye, in his debate with Ken Ham a couple years ago, talked about this very issue of the evolution of sexual reproduction. He started off by saying how it initially made no sense to scientists, because it was so inefficient when compared to asexual reproduction (there's a joke in there somewhere), but then they realized that it offered the chance at greater genetic diversity and could help in coping with disease. Because of this potential benefit, Bill Nye then said that sexual reproduction was a fulfilled prediction of evolution. Of course, Nye clearly didn't mean that sexual reproduction is a prediction of evolutionary theory in any specific sense. What Nye was saying was simply that evolution predicts that advantageous things will evolve. But this isn't true. Evolution doesn't predict that advantageous things will evolve. It predicts that, assuming all other things are equal, already evolved features will be selected if they are advantageous with respect to increased survival and reproduction. Explanations for the selection of features are not the same thing as explanations for the evolution of those features in the first place. Teleological explanations for the evolution of biological features are a blatant cheat, but they are used because they help sell the plausibility of evolutionary theory to the public. Noting that some feature confers a particular benefit is a perfectly reasonable explanation for why something would have been designed. It is not a reasonable explanation for why it would have been initially produced by a purposeless process that didn't have the benefit in view or the feature as a goal.
We reproduce sexually because we inherited this method from ancient ancestors. The ligitimate question of why we went down this evolutionarily less efficient method, is what science is trying to answer. I have no idea what an ID question looks like, therefore ID also has zero answers.
Um, an ID question would be identical, but would not simply assume that the feature exists in humans solely because it was inherited from some ancient ancestor and served no particular purpose in humans themselves. ID would also offer teleological answers that are not strictly confined to issues of reproductive fitness. And teleological answers under ID could actually serve as legitimate explanations for why some feature might have been designed and implemented, rather than simply selected for after it has managed to arrive on the scene through a series of happy accidents.HeKS
June 22, 2016
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TWSYF, can't really take credit for it. I shamelessly steal from others on UD and use their insights! :)bornagain77
June 22, 2016
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Bornagain77: Can't thank you enough for all of your comments, not just in this thread but in all threads on this site. Great work!Truth Will Set You Free
June 22, 2016
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We no longer say: “Another day; another bad day for Darwinism.” We now say: “Another day since the time Darwinism was disproved.” Love it!!!!Truth Will Set You Free
June 22, 2016
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'But they do. Well, a few do.' Take your dogma glasses off so you can read for comprehension for goodness sake. That concern was addressed.bornagain77
June 22, 2016
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ba77 @93 -
Besides the obvious problem for Darwinian theory that sexual reproduction is far less efficient than asexual reproduction, there is also the burning question, on the Darwinian perspective of ‘survival of the fittest’, of why bacteria don’t eat us.
But they do. Well, a few do.Bob O'H
June 22, 2016
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Moreover, there is very good reason to believe that pathogens were benign for most of their history and only recently became pathogenic
From friend to foe: How benign bacteria evolve to virulent pathogens, December 12, 2013 Excerpt: "Bacteria can evolve rapidly to adapt to environmental change. When the "environment" is the immune response of an infected host, this evolution can turn harmless bacteria into life-threatening pathogens. ...It is thought that many strains of E. coli that cause disease in humans evolved from commensal strains." http://medicalxpress.com/news/2013-12-friend-foe-benign-bacteria-evolve.html Setting a Molecular Clock for Malaria Parasites - July 8, 2010 Excerpt: The ancestors of humans acquired the parasite 2.5 million years ago. "Malaria parasites undoubtedly were relatively benign for most of that history (in humans), becoming a major disease only after the origins of agriculture and dense human populations," said Ricklefs. http://www.nsf.gov/news/news_summ.jsp?cntn_id=117259 "the AIDS virus originated relatively recently, as a mutation from SIV, the simian immuno-deficiency virus. According to Wikipedia, this virus was also benign in its original form:.. Unlike HIV-1 and HIV-2 infections in humans, SIV infections in their natural hosts appear in many cases to be non-pathogenic. Extensive studies in sooty mangabeys have established that SIVsmm infection does not cause any disease in these animals, despite high levels of circulating virus." https://uncommondescent.com/intelligent-design/macroevolution-microevolution-and-chemistry-the-devil-is-in-the-details/#comment-448372
Moreover, contrary to Darwinian thought, there is also good reason to believe that many pathogenic viruses and bacteria are caused by a loss of functional complexity not a gain. For instance, a genetic study has shown that bubonic plague (Black Death) was caused by loss of genes and streamlining (genetic entropy) of a non-pathogenic bacteria:
The independent evolution of harmful organisms from one bacterial family - April 21, 2014 Excerpt: "We commonly think bacteria must gain genes to allow them to become pathogens. However, we now know that the loss of genes and the streamlining of the pathogen's metabolic capabilities are key features in the evolution of these disease-causing bacteria," http://phys.org/news/2014-04-plague-family-independent-evolution-bacterial.html
Frankly, it is very good that there is a strict limit to what evolution can create, (Behe: 2 protein/protein binding site limit; Edge of Evolution), since it allows us to develop drug treatments that are beyond the capacity of Darwinian processes to overcome:
Guide of the Perplexed: A Quick Reprise of The Edge of Evolution - Michael Behe - August 20, 2014 Excerpt: If there were a second drug with the efficacy of chloroquine which had always been administered in combination with it (but worked by a different mechanism), resistance to the combination would be expected to arise with a frequency in the neighborhood of 1 in 10^40 -- a medical triumph. http://www.evolutionnews.org/2014/08/guide_of_the_pe089161.html
The multiple drug cocktail that has been so effective in controlling HIV uses much the same strategy of being beyond the 'edge of evolution' that Dr. Behe has elucidated:
When taking any single drug, it is fairly likely that some mutant virus in the patient might happen to be resistant, survive the onslaught, and spawn a resistant lineage. But the probability that the patient hosts a mutant virus that happens to be resistant to several different drugs at the same time is much lower.,,, it "costs" a pest or pathogen to be resistant to a pesticide or drug. If you place resistant and non-resistant organisms in head-to-head competition in the absence of the pesticide or drug, the non-resistant organisms generally win.,,, This therapy has shown early, promising results — it may not eliminate HIV, but it could keep patients' virus loads low for a long time, slowing progression of the disease. http://evolution.berkeley.edu/evolibrary/article/medicine_04
And it is also very good that genetic entropy is true. Sanford has shown that the destructive effects of pathogens on humans are fairly quickly are modulated by information loss.
Evolution and the Ebola Virus: Pacing a Small Cage - Michael Behe - October 24, 2014 Excerpt: The high rate of mutation of Ebola is similar to what John Sanford has demonstrated for the H1N1 virus that caused the influenza pandemic after World War I. He makes a compelling case that the accumulating mutations there were degradatory could not be eliminated easily by selection, and eventually caused the virus's extinction in 2009. http://www.evolutionnews.org/2014/10/evolution_and_t090621.html Biological Information - Positive Genetic Entropy (Mutational Meltdown, i.e. extinction, of pathogenic viruses over relatively short times) 2-7-2015 by Paul Giem - video https://www.youtube.com/watch?v=W17lVqYQzq4&list=PLHDSWJBW3DNUUhiC9VwPnhl-ymuObyTWJ&index=15
bornagain77
June 22, 2016
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Besides the obvious problem for Darwinian theory that sexual reproduction is far less efficient than asexual reproduction, there is also the burning question, on the Darwinian perspective of 'survival of the fittest', of why bacteria don't eat us. If evolution by natural selection were actually the truth about how all life came to be on Earth then the only ‘life’ that should be around would be extremely small organisms with the highest replication rate, and with the most 'mutational firepower', since only they, since they greatly outclass multi-cellular organism in terms of ‘reproductive success’ and 'mutational firepower', would be fittest to survive in the dog eat dog world where blind pitiless evolution ruled and only the fittest are allowed to survive. The logic of this is nicely summed up here in this Richard Dawkins video::
Richard Dawkins interview with a 'Darwinian' physician goes off track - video Excerpt: "I am amazed, Richard, that what we call metazoans, multi-celled organisms, have actually been able to evolve, and the reason [for amazement] is that bacteria and viruses replicate so quickly -- a few hours sometimes, they can reproduce themselves -- that they can evolve very, very quickly. And we're stuck with twenty years at least between generations. How is it that we resist infection when they can evolve so quickly to find ways around our defenses?" http://www.evolutionnews.org/2012/07/video_to_dawkin062031.html
In other words, since successful reproduction is all that really matters on a neo-Darwinian view of things, how can anything but efficient reproduction be realistically 'selected' for? Any other function besides efficient reproduction, such as much slower sexual reproduction, sight, hearing, thinking, etc.., would be highly superfluous to the primary criteria of efficient reproduction, and should, on a Darwinian view, be discarded, and/or 'eaten', by bacteria, as so much excess baggage since it would slow down efficient reproduction. Humorously, the real world example that Dawkins gave to Dembski, (in Dembski's critique of the hidden teleology within Dawkin's "WEASEL" program), illustrates exactly this point, i.e. the point that natural selection can only 'see' efficient reproduction and will 'discard' any excess baggage:
"Perhaps you should look at the work of Spiegelman and others on evolution of RNA molecules in an RNA replicase environment. They have found that, repeatedly, if you 'seed' such a solution with an RNA molecule, it will converge on a particular size and form of 'optimal' replicator, sometimes called Spiegelman's minivariant." Richard Dawkins to William Dembski http://www.evolutionnews.org/2012/08/conservation_of063671.html
Yet when we look at 'Spiegelman's minivariant' we find:
Spiegelman Monster is the name given to an RNA chain of only 218 nucleotides that is able to be reproduced by an RNA replication enzyme. It is named after its creator, Sol Spiegelman, of the University of Illinois at Urbana-Champaign. Spiegelman introduced RNA from a simple bacteriophage Q? (Q?) into a solution which contained Q?’s RNA replication enzyme, some free nucleotides, and some salts. In this environment, the RNA started to replicate. After a while, Spiegelman took some RNA and moved it to another tube with fresh solution. This process was repeated. Shorter RNA chains were able to replicate faster, so the RNA became shorter and shorter as selection favored speed. After 74 generations, the original strand with 4,500 nucleotide bases ended up as a dwarf genome with only 218 bases. Such a short RNA had been able to replicate very quickly in these unnatural circumstances. In 1997, Eigen and Oehlenschlager showed that the Spiegelman monster eventually becomes even shorter, containing only 48 or 54 nucleotides, which are simply the binding sites for the reproducing enzyme RNA replicase. http://www.revolvy.com/main/index.php?s=Spiegelman%20Monster In a classic experiment, Spiegelman in 1967 showed what happens to a molecular replicating system in a test tube, without any cellular organization around it. … these initial templates did not stay the same; they were not accurately copied. They got shorter and shorter until they reached the minimal size compatible with the sequence retaining self-copying properties. And as they got shorter, the copying process went faster. - Stephen Meyer - The Nature of Nature: Examining the Role of Naturalism in Science (Wilmington, DE: ISI Books, 2011), p. 313–18.
Needless to say, Dawkins real world example of 'Spiegelman's minivariant', i.e. loss of information to gain a reproductive advantage, to support his WEASEL program to Dembski is NOT what Dawkins needed to prove his point. But in actuality Dawkins' real world example proved Dembski's 'hidden teleology' critique of Dawkins' WEASEL to be right on the mark and also shows that 'survival of the fittest' is primarily concerned with efficient reproduction and nothing else. Moreover, contrary to this central 'survival of the fittest' assumption of Darwinian evolution, instead of eating us, time after time we find micro-organisms helping each other, and us, in ways that have nothing to with their own ‘survival of the fittest'’ concerns. The following researchers said they were ‘banging our heads against the wall' by the contradictory findings to Darwinian theory that they had found:
Doubting Darwin: Algae Findings Surprise Scientists - April 28, 2014 Excerpt: One of Charles Darwin's hypotheses posits that closely related species will compete for food and other resources more strongly with one another than with distant relatives, because they occupy similar ecological niches. Most biologists long have accepted this to be true. Thus, three researchers were more than a little shaken to find that their experiments on fresh water green algae failed to support Darwin's theory — at least in one case. "It was completely unexpected," says Bradley Cardinale, associate professor in the University of Michigan's school of natural resources & environment. "When we saw the results, we said 'this can't be."' We sat there banging our heads against the wall. Darwin's hypothesis has been with us for so long, how can it not be right?" The researchers ,,,— were so uncomfortable with their results that they spent the next several months trying to disprove their own work. But the research held up.,,, The scientists did not set out to disprove Darwin, but, in fact, to learn more about the genetic and ecological uniqueness of fresh water green algae so they could provide conservationists with useful data for decision-making. "We went into it assuming Darwin to be right, and expecting to come up with some real numbers for conservationists," Cardinale says. "When we started coming up with numbers that showed he wasn't right, we were completely baffled.",,, Darwin "was obsessed with competition," Cardinale says. "He assumed the whole world was composed of species competing with each other, but we found that one-third of the species of algae we studied actually like each other. They don't grow as well unless you put them with another species. It may be that nature has a heck of a lot more mutualisms than we ever expected. ",,, Maybe Darwin's presumption that the world may be dominated by competition is wrong." http://www.livescience.com/45205-data-dont-back-up-darwin-in-algae-study-nsf-bts.html
Moreover, instead of eating us, as would be expected an a Darwinian view, time after time different types of microbial life are found to be helping us in essential ways,,,
NIH Human Microbiome Project defines normal bacterial makeup of the body – June 13, 2012 Excerpt: Microbes inhabit just about every part of the human body, living on the skin, in the gut, and up the nose. Sometimes they cause sickness, but most of the time, microorganisms live in harmony with their human hosts, providing vital functions essential for human survival. http://www.nih.gov/news/health/jun2012/nhgri-13.htm We are living in a bacterial world, and it's impacting us more than previously thought - February 15, 2013 Excerpt: We often associate bacteria with disease-causing "germs" or pathogens, and bacteria are responsible for many diseases, such as tuberculosis, bubonic plague, and MRSA infections. But bacteria do many good things, too, and the recent research underlines the fact that animal life would not be the same without them.,,, I am,, convinced that the number of beneficial microbes, even very necessary microbes, is much, much greater than the number of pathogens." http://phys.org/news/2013-02-bacterial-world-impacting-previously-thought.html#ajTabs “Microbial life can easily live without us; we, however, cannot survive without the global catalysis and environmental transformations it provides.” - Paul G. Falkowski – Professor Geological Sciences – Rutgers
bornagain77
June 22, 2016
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Dr.JDD: If evolution is about survival and most likely to reproduce then it should have stopped at bacteria.
HeKS: It [sexual reproduction] offers an evolutionary advantage with respect to one set of considerations (genetic diversity) ....
The 'genetic diversity' argument doesn't work wrt bacteria: Andreas Wagner:
In another difference from sex as we know it, gene transfer occurs not just between similar organisms but also between baker’s yeast and fruit flies, between microbes and plants, and especially among bacteria, which can be as different from one another as humans are from oak trees.20 This is why gene transfer is so powerful, and the most important reason why bacteria are masters of metabolic innovation.
Origenes
June 22, 2016
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PaV - wrt novel genes, once more google is your friend. Again, first page of results. You're still punting the problem of gene loss/gain, so I guess we're done there. And I still haven't seen any maths from you about overcoming long odds, so I guess we're done there too.Bob O'H
June 22, 2016
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Arthur, this is from memory, and I only had the first two pages to look at: I believe their argument was that gene duplication allowed for that gene to lose part of its function. Then, when the original gene lost its promoter region function through a mutation within that region, then the new phenotype emerged. So, it's gene duplication at the service of 'gene loss.' No information is added, and then some is lost. And, overall, speciation occurs when this happens. Who would have thought? (Hope you're paying attention wd400)PaV
June 21, 2016
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Please type out your comment below. Bob O'H:
PaV: In the article I cited, they downplay the role of gene duplication. I think that’s a good idea.
Actually, they barely mention it, and make no comment on the relative importances. My guess is that they were asked to write a review about gene loss, and either decided comparing gene loss and gain would be too much, or had written something and were asked to take it out (to save space or not make the paper unwieldy).
If you read interviews of the authors, they seem to be very excited to have found a new way of looking at evolution, one driven by 'gene loss.'
PaV: As to “de novo” genes arising, the more critical question is how do “novel” genes arise, those that cannot be connected to other known sequences. How do you explain it, Bob?
By googling. And finding two papers that discuss just this. There are probably more too: these were from the first page of results.
But, Bob, those are about "de novo" genes, not "novel" genes, per se. "Novel" genes are a subset of "de novo" genes, and they don't match up to annotated genes; hence, their entire, sizable length have to be explained. Any ideas?
Pav: Who’s punting here, actually? Entropy is connected to information. All of science accepts this. Entropy is all about degrees of freedom. And, any nucleotide sequence has 4 degrees of freedom at each site. Do the math. It’s quite straightforward and easy. Bob O'H: Yes, I can count too. But so what? How does this relate to evolution, other than saying there is a very large genotype space? This is the problem I have – you can calculate these numbers, but I haven’t seen anything which suggests they’re meaningful with respect to evolution.
Isn't the real "problem" that you're accepting the "theory" of evolution as a "fact"? IOW, you say that when we look at organisms, their genomes are different, so we know that the 'long odds' against this happening are overcome. And, then, you attribute this to a purely materialistic mechanism. But that's an assumption. The only known "mechanism" of overcoming huge odds that we know of is the use of intelligence. That's a big part of what Stephen Meyer argues in "Darwin's Dilemna." You can't use what you assume to prove that which is in dispute.PaV
June 21, 2016
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You are correct HeKS, asexual reproduction is far more successful than sexual reproduction. That is why some plants, and some fungi, and all archaebacteria, eubacteria, and protists are far more abundent and therefore evolutionarily successful than us. It seems that everyone here is hell bent on asking, 'then why are we here, why are we so special?' If this is your question, then it sadly fails to understand Darwinian Evolution. We reproduce sexually because we inherited this method from ancient ancestors. The ligitimate question of why we went down this evolutionarily less efficient method, is what science is trying to answer. I have no idea what an ID question looks like, therefore ID also has zero answers. Bacteria reproduce asexually, they were probably the first life, they have existed for billions of years, and it is absolutely certain that when we dissapear, or destroy the planet, they will still be happily chugging along, and definately producing random gene errors that will possibly lead to the next sentient beings.rvb8
June 21, 2016
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Hmmm... If gene duplication doesn't add information, then the duplicates have no information. But if a duplicate is lost, then information is lost. That's some sort of funny math there.Arthur Hunt
June 21, 2016
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Dr JDD @74
So why did sexual reproduction even evolve? What advantage does it offer? What advantage does needing 2 separate individuals to have sexual relations actually bring to the table? If evolution is about survival and most likely to reproduce then it should have stopped at bacteria. They are far better at it than any multicellular organism. Plus they can do it in all sorts of environments – hot, cold, high salt, low salt, oxide, anoxic….
The belief is that sexual reproduction offers a chance at genetic diversity that is not offered by asexual reproduction, thereby giving the offspring of sexual reproduction a better chance at dealing with disease and potentially harmful microorganisms. That said, your point is completely valid. What we regularly see with evolutionary explanations for the arrival of some feature of biology is a description of some benefit it confers. The problem is that these sorts of explanations are blatantly teleological: Feature A evolved because it conferred advantage X. This might explain why a feature ended up being retained by natural selection after it arose, but it doesn't explain why the complex feature arose in the first place, unless we want to assign intelligence to evolution (as has been recently suggested). However, with regard to sexual reproduction, as you noted, it is far less efficient than asexual reproduction, so whatever advantages it confers, it carries some very significant evolutionary disadvantages as well. It offers an evolutionary advantage with respect to one set of considerations (genetic diversity), but an evolutionary disadvantage with respect to another set of considerations (reproductive success and larger populations). One wonders why the advantages should have outweighed the disadvantages in this case, since reproductive success is supposed to be the primary measure of fitness and main predictor of what traits will be passed on and fixed, while drastically reduced reproductive success and population sizes significantly decreases the potential for ongoing evolution in populations that rely on sexual reproduction. Meanwhile, asexually reproducing organisms may be more susceptible to disease and microorganisms, but they typically deal with these problems simply by having very large population sizes, and they are doing quite well to this day. So, in short, the reasons given for why sexual reproduction has hung around are dubious at best, considering reproductive success is supposed to be primary measure of fitness, but these reasons do nothing to explain why or how it actually arose in the first place.HeKS
June 21, 2016
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Alicia Cartelli:
Of course the researchers are going to make their work sound like the best thing since sliced bread while downplaying everyone else’s work. That’s what most research groups do, only to different degrees.
Alicia's posts are the best thing since sliced bread. Or at least they sound that way.Mung
June 21, 2016
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Bob O'H:
lots of things are sequences. But they can be produced in lots of different ways. Frankly, I have difficulty seeing how phone numbers mate and recombine, especially when within a longer string of sequences.
Ah, the old "I cannot imagine" defense. I could write a program in which phone numbers mate and recombine. Incredulity is not an explanation.Mung
June 21, 2016
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Bob O'H
lots of things are sequences. But they can be produced in lots of different ways. Frankly, I have difficulty seeing how phone numbers mate and recombine, especially when within a longer string of sequences.
How are sequences like phone numbers and languages produced? What happens if they are changed randomly?bill cole
June 21, 2016
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"The war is over. We won!" Whoever wrote this is very naive... One example comes to my mind when Jesus performed a miracle and yet the Jewish scribes while acknowledging his miracle they were still seeking to kill him... Why?J-Mac
June 21, 2016
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bill cole - lots of things are sequences. But they can be produced in lots of different ways. Frankly, I have difficulty seeing how phone numbers mate and recombine, especially when within a longer string of sequences.Bob O'H
June 21, 2016
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PaV @ 73 -
In the article I cited, they downplay the role of gene duplication. I think that’s a good idea.
Actually, they barely mention it, and make no comment on the relative importances. My guess is that they were asked to write a review about gene loss, and either decided comparing gene loss and gain would be too much, or had written something and were asked to take it out (to save space or not make the paper unwieldy).
As to “de novo” genes arising, the more critical question is how do “novel” genes arise, those that cannot be connected to other known sequences. How do you explain it, Bob?
By googling. And finding two papers that discuss just this. There are probably more too: these were from the first page of results.
Who’s punting here, actually? Entropy is connected to information. All of science accepts this. Entropy is all about degrees of freedom. And, any nucleotide sequence has 4 degrees of freedom at each site. Do the math. It’s quite straightforward and easy.
Yes, I can count too. But so what? How does this relate to evolution, other than saying there is a very large genotype space? This is the problem I have - you can calculate these numbers, but I haven't seen anything which suggests they're meaningful with respect to evolution.Bob O'H
June 21, 2016
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Some people take it very personal when their world view is challenged.Andre
June 21, 2016
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